PubMed · 13701408
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J FRANKEL. 1961. Ophthalmodynamometry: a pilot study.. https://pubmed.ncbi.nlm.nih.gov/13701408/
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OBJECTIVE: Elevation of blood pressure and heart rate increase the risk of cardiovascular disease. Administration of estrogens does not affect heart rate but may decrease 24 h blood pressure. In this study, we tested the effect of the estro-progestogenic compound tibolone. METHODS: Thirty healthy, post-menopausal women were randomized to receive placebo (n = 15) or tibolone, at the commonly prescribed dose of 2.5 mg per day (n = 15). Before and after 6 months of treatment, in each woman blood pressure and heart rate were monitored every 30 min for 41 h by an ambulatory device. Valuable readings were those collected from 8:00 a.m. of the second day to 8:00 a.m. of third day. Analyses were performed of 24 h, day-time (7:00 a.m.-11:00 p.m.) and night-time (11:00 p.m.-7:00 a.m.) values. Day to night difference was also calculated. RESULTS: Placebo did not modify 24h, day-time, and night-time blood pressure or heart rate values. Day-night differences were also not affected by placebo. Similarly to placebo, tibolone administration did not modify any of the blood pressure parameters taken into consideration. By contrast, a significant decline of 24 h heart rate (73.2 +/- 2.3 beats/min versus 69.3 +/- 1.7 beats/min; P < 0.0008) was observed. The effect was significant both at day (76.6 +/- 2.4 beats/min versus 72.1 +/- 1.9 beats/min; P < 0.0001) and night (65.8 +/ 2.6 beats/min versus 62.4 +/- 1.9 beats/min; P < 0.05). Day-night blood pressure and heart rate differences were not affected by tibolone. CONCLUSIONS: In post-menopausal women, administration of tibolone does not influence 24 h blood pressure but reduces heart rate.
BACKGROUND: Small studies have reported that vasopressin improves hemodynamic instability in patients with septic shock. OBJECTIVE: To determine whether vasopressin infusion increases blood pressure, decreases catecholamine vasopressor use, and improves renal function in a large patient population with septic shock when used in a clinical setting. METHODS: A retrospective chart audit was conducted of critically ill patients who received vasopressin infusion for septic shock from January 2000 through September 2002. Demographic, hemodynamic, laboratory, vasopressor, and adverse event data were collected. Statistical methods included ANOVA with Tukey's test for post hoc analysis. RESULTS: A total of 102 of 353 patients met study criteria. The mean +/- SD vasopressin dosage regimen was 0.11 +/- 0.17 units/min for 53.8 +/- 71.5 hours. Compared with baseline, vasopressin infusion improved mean arterial pressure (MAP) by 15% within one hour (p < 0.05), reduced heart rate by 9% within 4 hours (p < 0.05), and reduced hourly dopamine dosage by 25% within 8 hours (p < 0.05). These effects persisted through 96 hours. Other hemodynamic variables and catecholamine vasopressor usage parameters were not statistically different from baseline. Urine output, serum creatinine, and serum sodium concentrations were not statistically changed from baseline. Adverse events possibly associated with vasopressin infusion included ischemic digits/extremities, myocardial infarction, and hyponatremia. CONCLUSIONS: Vasopressin infusion was effective in increasing MAP and reducing heart rate while decreasing the dopamine dosage in patients with septic shock. Comparative studies with catecholamine vasopressors are needed to define the optimal role of vasopressin in septic shock therapy. In the meantime, vasopressin infusion at <or=0.03 units/min should be considered only if response to 1 or 2 catecholamine vasopressors is inadequate or as a method to reduce the dose of these therapies.
BACKGROUND: The regulation of renal sympathetic activity in the setting of heart failure is largely unexplored. We used the norepinephrine spillover method to address the hypothesis that baroreflex control of renal sympathetic activity is blunted in heart failure. METHODS AND RESULTS: Twenty-two patients were studied, 11 in a group with heart failure and 11 in a group with normal ventricular function. In both groups, renal norepinephrine spillover was assessed in response to sodium nitroprusside infused to steady-state conditions. Sodium nitroprusside resulted in significant reductions in mean systemic arterial pressure (normal group, -13+/-1% [mean+/-SEM]; heart failure group, -12+/-1%). In response to nitroprusside, there was an 85+/-34% increase in renal norepinephrine spillover in the normal group (from 537+/-84 to 840+/-140 pmol/min, P<0.05). Despite similar hemodynamic responses to nitroprusside in the heart failure group, renal norepinephrine spillover was unchanged (from 1420+/-153 to 1387+/-161 pmol/min, P=NS), a response that was significantly different from that seen in the normal group. CONCLUSIONS: In patients with heart failure, compared with those with normal ventricular function, renal sympathetic activity did not change in response to a steady-state infusion of sodium nitroprusside. This result provides evidence for reduced baroreflex control of renal sympathetic activity in heart failure.